Evidence map›Paper›PMID 39796274›Full record

ReviewInternational journal of molecular sciences2025

The Fetal Environment and the Development of Hypertension-The Epigenetic Modification by Glucocorticoids.

Fumiko-Kawakami Mori, Tatsuo Shimosawa

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Fumiko-Kawakami MoriDepartment of Endocrinology, Mitsui Memorial Hospital, Tokyo 101-8643, Japan.
Tatsuo ShimosawaDepartment of Clinical Laboratory, School of Medicine, International University of Health and Welfare, Otawara 324-8501, Japan.ORCID 0000-0002-8742-5129

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intrauterine growth restriction (IUGR) is a risk factor for postnatal cardiovascular, metabolic, and psychiatric disorders. In most IUGR models, placental dysfunction that causes reduced 11β-hydroxysteroid dehydrogenase 2 (11βHSD2) activity, which degrades glucocorticoids (GCs) in the placenta, resulting in fetal GC overexposure. This overexposure to GCs continues to affect not only intrauterine fetal development itself, but also the metabolic status and neural activity in adulthood through epigenetic changes such as microRNA change, histone modification, and DNA methylation. We have shown that the IUGR model induced DNA hypomethylation in the paraventricular nucleus (PVN) in the brain, which in turn activates sympathetic activities, the renin-angiotensin system (RAS), contributing to the development of salt-sensitive hypertension. Even in adulthood, strong stress and/or exogenous steroids have been shown to induce epigenetic changes in the brain. Furthermore, DNA hypomethylation in the PVN is also observed in other hypertensive rat models, which suggests that it contributes significantly to the origins of elevated blood pressure. These findings suggest that if we can alter epigenetic changes in the brain, we can treat or prevent hypertension.

Indexed as

DNA MethylationEpigenesis, GeneticGlucocorticoidsHypertension11-beta-Hydroxysteroid Dehydrogenase Type 2AnimalsFemaleFetal Growth RetardationHumansPregnancyRenin-Angiotensin System11-beta-Hydroxysteroid Dehydrogenase Type 2Glucocorticoidsblood pressuredevelopmental origins of health and disease (DOHaD)DNA methylationenvironmentepigeneticshypothalamus

Identifiers

PMID39796274
PMCPMC11720225

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.